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Lukong, K. E.

Publications and source records attributed to Lukong, K. E..

2 recordsLinked to original sources

Systemic Genome Correlation Loss as a Central Characteristic of Spaceflight

Spaceflight exposes the human body to a unique combination of stressors--microgravity, radiation, and confinement--that induces multisystemic physiological dysregulation. Traditional transcriptomic analyses have focused on differential expression to identify key genes, yet this approach fails to explain why astronauts experience systemic fragility despite often subtle changes in gene abundance. Here, we present a comprehensive meta-analysis of 10 independent transcriptomic and genomic datasets (N = 136) from the NASA Open Science Data Repository. By shifting focus from gene abundance to gene-gene correlation topology, we identify Systemic Genome Correlation Loss as a central biosignature of spaceflight. We show that the regulatory architecture of the transcriptome undergoes a profound decoherence in microgravity, shifting the global correlation distribution toward stochasticity (p < 10-15). This phenomenon is universal across tissues and independent of gene variance. We identify a massive population of 760 genes that maintain stable expression levels but lose over 500 regulatory connections each, outnumbering canonical differentially expressed genes by three-to-one. Finally, we demonstrate that cells preserve the connectivity of survival-critical DNA repair networks preferentially while allowing mitochondrial and synaptic networks to shatter. These findings suggest that astronaut health risks are driven by the entropic decay of regulatory synchronization, proposing a new paradigm for countermeasure development focused on network stabilization rather than pathway inhibition.

genomics↗

Rewiring of a SMAD4 Protein Interaction Network by Breast Tumor Kinase Mediated Phosphorylation

The tumor-suppressing function of SMAD4 is frequently subverted during mammary tumorigenesis, leading to cancer growth, invasion, and metastasis. A long-standing concept is that SMAD4 is not regulated by phosphorylation but ubiquitination. Interestingly, our search for signaling pathways regulated by BRK, a non-receptor protein tyrosine kinase that is up-regulated in [~]80% of invasive ductal breast tumors, led us to discover that BRK competitively binds and phosphorylates SMAD4, and regulates TGF-{beta}/ SMAD4 signaling pathway. A constitutively active BRK (BRK-Y447F), phosphorylates SMAD4 resulting in its recognition by the ubiquitin-proteasome system, which accelerates SMAD4 degradation. In agreement, we also observed an inverse protein expression pattern of BRK and SMAD4 in a panel of breast cancer cell lines and breast tumors. Activated BRK mediated degradation of SMAD4 causes the repression of tumor suppressor genes FRK that was associated with increased expression of mesenchymal markers and decreased cell adhesion ability. Thus, our data suggest that combination therapies targeting activated BRK signaling may have synergized the benefits in the treatment of SMAD4 repressed cancers. Therefore, our data propose that combination therapies which includes targeting activated BRK signaling may synergize the benefits in the treatment of SMAD4 deficient cancers.

cancer biology↗